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Clinical sciences > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is angina?

A

Chest pain when blood flow to coronary arteries is restricted. It is a symptom of restricted blood flow.

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2
Q

What is the main cause of angina?

A

Atherosclerosis

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3
Q

What are the 3 main coronary arteries?

A

Right coronary artery
Circumflex artery
Left anterior descending

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4
Q

What is Pouiselle’s law?

A

Resistance α 1/radius^4

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5
Q

In a healthy individual at rest is the resistance of the epicardial vessels and microvasculature low medium or high?

compared to a diseased individual at rest?

A

Epicardial vessels = low
Microvasculature = medium

Diseased-
Epicardial vessels = high
Microvasculature = lower(compensating)

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6
Q

What is the average flow rate of blood in coronary arteries? and what can it increase to in exercise?

A

3ml/s

Above 15ml/s

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7
Q

What are the main non modifiable risk factors for angina?

A

Gender, age, family history

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8
Q

What are the main modifiable risk factors for angina?

A

Smoking, hypertension, diabetes, hypercholesterolaemia, sedentary lifestyle, stress(less)

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9
Q

What is the main clinical feature of angina?

A

Chest pain

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10
Q

What are the 3 key points used to score angina /3?

A
  1. Central heavy pain, tight/radiating to arm/jaw/neck
  2. Pain precipitated by exertion
  3. Pain relieved by rest

3/3 = typical angina
2/3 = atypical pain
1 or less/3 = non anginal pain

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11
Q

What are the main differential diagnoses of angina?

A

Pericarditis/PE/pleurisy/chest infection/ dissection of aorta

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12
Q

On examination how may a patient with stable angina present?

A

Often normal

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13
Q

What ‘sign’ do you look out for in patients with angina?

A

Levine sign (clenched fists over chest)

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14
Q

What are the two basic investigations done when a patient has suspected angina and what is seen?

A
  1. ECG - Can be normal (between attacks) or show resting ST segment depression/ T wave flattening or inversion
  2. Echo - often normal. May be signs of previous infarcts, long Q waves, T wave inversion, BBB
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15
Q

What is the definition of hypertension? (value)

A

140/90mmHg based on at least two readings on separate occasions/ ambulatory blood pressure monitoring (24 hrs)

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16
Q

Hypertension is a major risk factor for what?

A

Stroke, MI, HF, renal disease, cognitive decline

Also increases risk of AF

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17
Q

Give the equation for blood pressure

A

BP = CO x TPR

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18
Q

What two factors play a big role in determining CO and TPR and therefore blood pressure?

A
  1. Renin-angiotensin-aldosterone system

2. Sympathetic nervous system(NA)

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19
Q

What affect does Angiotensin II have on the systemic circulation?

A

Potent vasoconstrictor

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20
Q

What effect does aldosterone have on tubular reabsorption/excretion of ions?

A

Reabsorbs sodium and chloride

Secretes potassium

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21
Q

How do ACE - inhibitors work?

A

Reduce convertion of angiotensin I to angiotensin II

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22
Q

What conditions are ACE-inhibitors used in?

A
  1. Hypertension
  2. Heart failure
  3. Diabetic neuropathy
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23
Q

What conditions are ACE-inhibitors contraindicated in?

A

Renal artery stenosis and preganacy (teratogenic)

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24
Q

Give 2 examples of ACE-inhibitors?

A

Ramipril, enalapril

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25
Q

What are the adverse effects of ACE-inhibitors?

A
  1. Decrease in angiotensin II causes hypotension, vasodilation of efferent arteriole and therefore acute renal failure, hyperkalaemia and is teratogenic
  2. Increased kinin production causes a dry cough in 10%, a rash and anaphylactoid reaction
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26
Q

Why do ACE inhibitors cause increase kinin production, and what effect does this have on systemic circulation?

A

ACE converts angiotensin I –> angiotensin II alongside bradykinin being converted into inactive peptides, so builds up as is no longer being converted

Bradykinin is a vasodilator

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27
Q

What is the main cause for the use of angiotensin II receptor blockers? (ARB)

A

If ACE-inhibitor contraindicated (i.e. causes a cough)

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28
Q

In what conditions are ARB’s used in?

A
  1. Hypertension
  2. HF
  3. Diabetic neuropathy
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29
Q

Give 2 examples of ARB’s

A
  1. Losartan

2. Candesartan

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30
Q

What are the main adverse effects of ARB’s?

A
  1. Symptomatic hypotension
  2. Hyperkalaemia
  3. Potential renal dysfunction
  4. Rash
  5. Angioedema (result of allergic reaction)
  6. CONTRAINDICATED IN PREGNANCY
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31
Q

How do angiotensin II receptor blockers (antagonists) work?

A

Selectively block receptor for angiotensin II (AT-1 receptor) meaning little aldosterone production.

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32
Q

What conditions are calcium channel blockers used in?

A
  1. Hypertension
  2. IHD (angina)
  3. Arrhythmia (tachy)
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33
Q

How do calcium channel blockers work?

A

Block L-type calcium channels and modify calcium uptake into myocardium and vascular smooth muscle.

Dihydropyridines are potent vasodilators with little effect on cardiac contractility or conduction

Verapamil/diltiazem are weak vasodilators but depress cardiac conduction and contractility

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34
Q

What are the 3 classes of calcium channel blockers and give at least one example of each alongside how they work

A

Dihydropyridines: Vasodilator e.g. amlodipine, nifedipine, felodipine
Phenylalkylamines: Negatively inotropic and chronotropic e.g. verapamil
Benzothiazepines: Intermediate heart and peripheral vascular effects e.g. diltiazem

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35
Q

Define chronotropic and inotropic

A

Chronotropic- Alters heart rate

Inotropic - Alters force or energy of cardiac contraction

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36
Q

What are the adverse effects of calcium channel blockers (calcium antagonists)?

A
  1. Due to peripheral vasodilation: flushing, oedema, headache, palpitations (dihydropyridines)
  2. Due to negatively chronotropic effects: Bradycardia, AV block (verapamil/ diltiazem)
  3. Due to negatively inotropic effects: worsening HF (verapamil/diltiazem)

Verapamil can also cause constipation

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37
Q

How do beta blockers work?

A

They block the B-adrenoreceptors in the heart, peripheral vasculature, bronchi, pancreas and liver.

This decreases heart rate (negatively chronotropic) Reduces the force of cardiac contraction (negatively inotropic) - reduce myocardial oxygen demand and give more time for perfusion
Lowers blood pressure

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38
Q

In what conditions are beta blockers used?

A
  1. IHD (angina)
  2. HF
  3. Arrhythmia
  4. Hypertension
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39
Q

Which beta blockers are classified as B1 selective?

A

Metoprolol

Bisoprolol (potentially atenolol but is more central)

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40
Q

Which beta blockers are classified as non selective?

A

Propanolol
Nadolol
Carvedilol

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41
Q

What happens to the selectivity of beta blockers at high doses?

A

Selectivity is lost

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42
Q

What is meant by the term ‘cardioselective’?

A

Implies B1 selectivity

However, up to 40% of cardiac B-adrenoreceptors are actually B2 receptors

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43
Q

What are the main adverse effects of beta blockers?

A
  1. Fatigue, headache, sleep disturbance/nightmares
  2. Bradycardia, hypotension, cold peripheries, erectile dysfunction
  3. Worsening of asthma, PVD, HF (if given standard dose/acutely)
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44
Q

In what conditions are beta blockers contraindicated?

A 
Asthma 
HF (in standard dose- if given in v.v. small doses is actually the treatment of HF)
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45
Q

How do diuretics work?

A

Reduce sodium and chloride reabsorption at different sites in the nephron and thus increase urinary sodium and water loss.

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46
Q

In what conditions are diuretics used?

A
  1. Hypertension

2. Heart failure

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47
Q

What are the 3 classes of diuretic and how do they work?

A
  1. Thiazides + related (distal tubule also reduce peripheral vascular resistance)
  2. Loop diuretics (loop of Henle and increase venous capacitance (helps acute HF))
  3. Potassium sparing diuretics/aldosterone receptor antagonist - don’t cause hypokalaemia so can be used in conjunction with loop or thiazide diuretics
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48
Q

Give an example of each of a drug in each of the 3 main classes of diuretics

A
  1. Thiazides - Bendroflumethiazide
  2. Loop diuretics - Furosemide
  3. Potassium sparing/aldosterone antagonist - Spironolactone
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49
Q

What are the main adverse effects of diuretics?

A
  1. Hypovolaemia or hypotension (loop)
  2. Low serum potassium, sodium, magnesium, calcium
  3. Raised uric acid (can lead to gout)
  4. Erectile dysfunction (thiazides)
  5. Impaired glucose tolerance (thiazides)
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50
Q

What are the 3 classes of antihypertensives that are

smaller and give an example of each

A
  1. Alpha-1 adrenoreceptor blockers (doxazosin)
  2. Centrally acting antihypertensives (methyldopa)
  3. Direct renin inhibitor (aliskiren)
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51
Q

Patient under 55 presents with hypertension. What is the first step taken in their treatment?

A

ACE inhibitor (or ARB)

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52
Q

Patient aged 55 or over presents with hypertension. What is the first step taken in their treatment?

A

Calcium channel blocker

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53
Q

43 year old afro-Caribbean patient presents with hypertension. What is the first step taken in their treatment?

A

Calcium channel blocker

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54
Q

Patient with hypertension presents, they have had first stage treatment but it hasn’t been effective. What happens now?

A

Prescribe ACE inhibitor/ARB and calcium channel blocker

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55
Q

Patient presents with hypertension. They are currently on both a ACE inhibitor and a calcium channel blocker. What is the next step in their treatment?

A

Add a thiazide like diuretic

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56
Q

Patient presents with hypertension. They are currently on ACE inhibitor, calcium channel blocker and thiazide like diuretic. What is the next step in their treatment?

A

Add either:

Spironolactone, alpha blocker, beta blocker or high dose thiazide like diuretic

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57
Q

What is heart failure?

A

Complex clinical syndrome of signs and symptoms that suggest the efficiency of the heart as a pump is impaired

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58
Q

What are the two types of heart failure and which is the most common?

A

HF due to left ventricular systolic dysfunction (LVSD)
HF due to preserved ejection fraction (diastolic failure) (HFPEF)

Most common is LVSD

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59
Q

What is the most common cause of HF?

A

Coronary artery disease

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60
Q

In heart failure, what has been shown to be the most useful type of therapy?

A

Neurohumoral blockade (RAAS-SNS) - blocking these

NOT/ Direct LV stimulation

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61
Q

In HF, what class of drugs are prescribed to treat congestion?

A

Diuretics (usually loop)

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62
Q

Alongside diuretics (to treat congestion) what would be the first line of treatment in a patient with HF?

A

ACE inhibitor + beta blocker (low dose and very slow uptitration)

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63
Q

What drug or combination of drugs would be used in a patient with heart failure if they were both ACE-I and ARB intolerant?

A

Hydralazine/nitrate combination

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64
Q

What hormones are released by the heart when atrial and ventricular muscle cells are stretched or there is raised atrial and ventricular pressure?

A

Atria - Atrial natriuretic peptide

Ventricles - Brain natriuretic peptide

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65
Q

What are the main effects of the hormones ANP and BNP released by the heart?

A
  1. Increase renal excretion of sodium and water
  2. Relax vascular smooth muscle (except efferent arterioles)
  3. Increased vascular permeability
  4. Inhibits release or effects of aldosterone, angiotensin II, endothelin and ADH
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66
Q

What hormones work against the renin angiotensin system?

A

Cardiac natriuretic peptides

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67
Q

How can levels of cardiac natriuretic peptides be manipulated to provide therapy for heart failure?

A

CNP’s are metabolised by NEP (neprilysin)
NEP inhibition increases their levels
Entresto does this

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68
Q

How do nitrates work and what conditions do they treat?

A

Are arterial and venous dilators, so reduce preload and afterload
Lower BP

Used in IHD (angina) and HF

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69
Q

What are the main side effects of nitrates?

A

Headache, GTN syncope

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70
Q

What are the main differences between chronic stable angina and unstable angina?

A

Chronic stable = occurs on exertion, infrequent

Unstable = unpredictable, frequent, may occur at rest

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71
Q

What classes of drugs would you prescribe in chronic (stable) angina?

A
  1. Antiplatelet therapy (aspirin or clopidogrel)
  2. Lipid-lowering therapy - statins (simvastatin)
  3. Short acting nitrate (acute attack) - GTN
  4. First line treatment for cause of angina - Beta blocker or calcium channel blocker
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72
Q

What classes of drugs would you prescribe in acute coronary syndromes? (NSTEMI and STEMI)

A
  1. Dual antiplatelet therapy (Aspirin + clopidogrel)
  2. Lipid lowering therapy (statin)
  3. Antithrombin therapy: Fondaparinux
  4. Background angina therapy - BB, CCB
  5. Pain relief- GTN spray and opiates (diamorphine)
  6. HIGH RISK- Glycoprotein inhibitor (tirofiban)
  7. Therapy for LVSD as req’d - ACE-I, BB, Aldosterone antagonist
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73
Q

What are the 4 main classes of antiarrhythmic drugs?(Vaughan Williams classification)

A

Class 1: Sodium channel blockers
Class 2: Beta adrenoreceptor antagonists
Class 3: Prolong AP (amiodarone)
Class 4: Calcium channel blockers (verapamil, diltiazem)

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74
Q

What are the two most prevalent causes underlying coronary thrombosis?

A
  1. Plaque rupture

2. Plaque erosion

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75
Q

What are the major cell types involved in atherosclerosis?

A

Endothelium, macrophages, smooth muscle cells and platelets

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76
Q

What are the risk factors for atherosclerosis?

A

Age, tobacco smoking, high serum cholesterol, obesity, diabetes, hypertension, family history

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77
Q

What are the 3 factors involved in Virchow’s triad?(thrombosis)

A
  1. Endothelial injury
  2. Hypercoagulability
  3. Stasis of blood flow (changes)
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78
Q

How is inflammation on the arterial wall ignited?

A

LDL’s accumulate on the wall and are modified by oxidation.
This inflames endothelial cells
Endothelial cells then release chemoattractants which attract macrophages, which are transmigrated into intima.

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79
Q

What is the term used for the first signs of atherosclerosis. What cells do these lesions include?

A

Fatty streaks

Include lipid laden macrophages (foam cells) and T lymphocytes in intima

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80
Q

How are intermediate lesions in atherosclerosis different from fatty streaks?

A

Include vascular smooth muscle cells from media.

Also have platelets beginning to aggregate to them

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81
Q

What is the term given to lipid laden macrophages in atherosclerosis?

A

Foam cells

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82
Q

The fibrous cap formed in advanced lesions of atherosclerosis is made from extracellular matrix proteins (collagen and elastin). What cells lay down this fibrous cap?

A

Smooth muscle cells

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83
Q

Why must the fibrous cap be resorbed and redeposited in order to be maintained?

A

Is a balance between T lymphocytes interacting with macrophages and resorbing the cap, and new collagen and elastin being layed down by smooth muscle cells

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84
Q

How are advanced lesions in atherosclerosis different to both intermediate lesions and fatty streaks?

A

Include a fibrous cap made of elastin and collagen (+ other ECM cells)

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85
Q

What is the difference between plaque erosion and plaque rupture?

A

Thrombus in plaque rupture is red vs. in plaque erosion is white (neutrophils)

Plaque erosion is not assosciated with high cholesterol (LDL) and the fibrous cap is not disrupted

However mechanism is unknown

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86
Q

What does PCI stand for and what is the main form of PCI treatment?

A

Percutaneous coronary intervention

Stenting

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87
Q

If an electrical wave of depolarisation is travelling towards an electrode what kind of deflection is seen?

A

Positive (opposite if is a wave of repolarisation)

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88
Q

State the 5 steps of impulse conduction in the heart beginning at SA node

A
  1. Sinoatrial node
  2. AV node
  3. Bundle of His
  4. Bundle branches
  5. Purkinje fibres
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89
Q

Why can the T wave not normally be seen on an ECG?

A

Occurs at the same time as QRS

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90
Q

What is the PR interval?

A

Start of P to start of QRS

Is the atrial depolarisation + delay in the AV junction (AV node to bundle of His)- this allows for the atria to contract before ventricles

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91
Q

What is the QT interval?

A

Start of Q until end of T

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92
Q

What is the difference between limb leads and precordial leads?

A

The limb leads are bipolar, so is measuring the difference in electrical potential between these two points

The precordial leads are all placed around the heart and are unipolar leads, their electrical potential is compared to that of a virtual reference point (0) in the centre of the heart

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93
Q

What is the difference between standard limb leads and augmented limb leads?

A

Augmented limb leads use the same electrodes as standard limb leads, but instead of the negative pole being a single electrode, it is a combination of both of the remaining electrodes.

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94
Q

What do aVL, aVR and aVF stand for?

A 
aVL = augmented vector left
aVR = augmented vector right
aVF = augmented vector foot
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95
Q

Where are each of the 6 precordial electrodes placed?

A

V1 4th intercostal space right of sternum
V2 4th intercostal space left of sternum
V3 Between V2 and V4
V4 5th intercostal space mid clavicular line
V5 Horizontal with V4 anterior axillary line
V6 Horizontal with V4 and V5 mid axillary line

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96
Q

What are the 10 rules in an ECG?

A
  1. QRS should be less than 3 small squares <110ms
  2. QRS should be dominantly upright in leads I and II
  3. QRS and T waves should be in the same direction in all limb leads
  4. P waves should be upright in leads I, II, V2-6
  5. PR segment should be between 3 and 5 small squares (120-200ms)
  6. T waves should be upright in leads I,II and V2-6
  7. ST segment should be isoelectric or slightly elevated in V1-2
  8. R wave should grow between V1-V4 and S wave should grow between V1 and V3 and not be present in V6
  9. There should be no Q wave in leads I,II or v2-6 (or less than 1 small square)
  10. All aVR waves should be negative
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97
Q

On ECG, P wave appears bifid or notched. What is this an indication of?

A

P.mitrale = Left atrium enlargement

Can be caused to mitral stenosis (narrowing of valve) or hypertension (systemic)

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98
Q

On ECG, P wave appears tall and peaked (>2.5mm). What is this an indication of?

A

P.pulmonale = Right atrium enlargement

Due to pulmonary hypertension or COPD/emphysema

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99
Q

If on ECG there is a short PR interval, what condition may the individual have?

A

Wolff-Parkinson-White syndrome

Has an accessory ‘bundle of Kent’ which allows early excitation of the ventricle

Individual may have bouts of tachycardia

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100
Q

What is a long PR interval suggestive of?

A

First degree heart block

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101
Q

If there is no initial downwards dip in the QRS segment, what is the first peak called?

A

R

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102
Q

What is a broad QRS complex suggestive of? >2.5 squares

A

Bundle branch block

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103
Q

If a patient had left ventricular hypertrophy what would been seen on their ECG?

A

Tall R waves in LV leads (v5+6) or deep S waves in RV leads (v1+2)

Sum would be greater than 40mm

104
Q

If a patient had right ventricular hypertrophy what would be seen on their ECG?

A

Tall T waves in RV leads (v1+2) or deep S waves in LV leads (v5+6)

Sum would be greater than 40mm

105
Q

ST segment is normally isoelectric

What does it suggest if not?

A 
Elevation = MI/acute pericarditis
Depression = Ischaemia

> 1mm

106
Q

What is the QT interval, what is a normal QT interval and what does long QT interval give an increased risk of?

A

Start of QRS to end of T

Normal = 0.35-0.45 seconds

Long QT syndrome = increased risk of torsades de pointes and sudden death

107
Q

Explain the two methods you can use to work out heart rate from an ECG

A
  1. Rule of 300- for regular rhythms. Count number of big boxes between QRS and divide 300 by this
  2. 10 second rule - for irregular beats - ECG’s record 10 seconds of rhythm per page, so count number of beats present and x 6
108
Q

What does the QRS axis represent?

A

The overall direction of the heart’s electrical activity

109
Q

What does a normal QRS axis range from and to?

A

-30 degrees to +90 degrees

110
Q

What is left axis deviation?

A

-30 degrees to -90 degrees

111
Q

What is right axis deviation?

A

+90 degrees to +180 degrees

112
Q

If an M or W is seen in ECG in leads V1 or V6 what is it suggestive of ?

A

M v1 = RBBB

M in v6 = LBBB

113
Q

What are you looking for on ECG during a treadmill test to confirm angina/ stable CAD

A

ST segment depression

114
Q

A CT angiogram has a high NPV and a low PPV. What does this mean it is useful in?

A

Good for exclusing CAD in younger, lower risk patients.

115
Q

How would a positive stress echo appear on screen?

A

One side of the heart may stop working as much as the other

116
Q

How does SPECT work?

A
  1. Stress heart using drug (adenosine) and insert tracer- is taken up by metabolising tissues
  2. Look at scan, if there is a perfusion defect then bring back for a second scan under resting conditions
  3. If the perfusion defect goes on rest then it shows ischaemia, but if it remains is likely to be a scar
117
Q

What tool is used to predict the 10 year risk of a major CV event?

A

SCORE

118
Q

Name 3 categories of drugs that are first line antianginals

A
  1. Beta blockers
  2. Nitrates
  3. Calcium channel blockers
119
Q

What is the difference between primary and secondary prevention?

A

Primary prevention consists of risk factor modification, before a CV event occurs

Secondary prevention takes place after a CV event has occurred, in an attempt to prevent another as well as manage symptoms.

120
Q

Why are calcium channel antagonists used as first line antianginals alongside beta-blockers and nitrates?

A

Are ARTERODILATORS (lowers blood pressure) (dihydropyridines)

Meaning that the afterload (pressure against which LV must pump to eject blood) is reduced

So reduce work of the heart and O2 demand

Verapamil/diltiazem are directly negatively inotropic

121
Q

Why are beta blockers used as first line antianginals alongside calcium channel antagonists and nitrates?

A

Bind to B1 adrenoreceptors, in heart and are negatively chronotropic and inotropic

122
Q

Why are nitrates used as first line antianginals alongside calcium channel blockers and beta blockers?

A

Nitrates are venodilators
Dilate systemic veins and so reduce venous return to R of heart
Reduces preload so via Frank Starling can see that work of heart is reduced

123
Q

What are the main two categories of drugs that will actively decrease prognosis of a CV event in an individual that suffers with angina?

A
  1. Antiplatelets (e.g. aspirin)

2. Statins (e.g. simvastatin)

124
Q

How does aspirin work as antiplatelet therapy as well as an an analgesic?

A

It inhibits COX-1 which inhibits platelet generation of thromboxane-A2 at lower doses

At higher doses it binds and inactivates COX-1 and 2, which blocks prostaglandin production, having an analgesic effect.

125
Q

What are the two methods of revascularisation and are the main pros and cons of each?

A
  1. PCI - less invasive, fast recovery time but possibility of restenosis and need dual antiplatelet therapy
  2. CABG- Long recovery, invasive, but can deal with complex disease and has good prognosis
126
Q

What 2 things classify angina as unstable?

A
  1. Cardiac chest pain at rest
  2. Cardiac chest pain with crescendo pattern
  3. New onset angina
127
Q

What is the significance of a positive troponin test?

A

Suggests an MI in last 6 hours-2 weeks

or other cardiac damage

128
Q

What clinical findings would suggest a larger infarct and therefore a higher chance of pathological Q wave formation, heart failure and death?

A

ST elevation

LBBB

129
Q

ST elevation is suggestive of what?

A

MI - in aVL can also be caused by pericarditis

130
Q

What are the classic symptoms of MI?

A
  1. Unremitting cardiac chest pain (occurring at rest)
  2. Sweating
  3. Breathlessness
  4. Nausea and vomiting
131
Q

Why does heart failure cause salt and water retention (and therefore oedema)?

A

Low renal perfusion

132
Q

Define pericardial tamponade

A

When fluid builds up in the pericardium and results in pressure on the heart

133
Q

What in the normal amount of fluid in the pericardium, and what is the pericardium made from?

A

50ml

Acellular collagen and elastin fibres

134
Q

What is the purpose of pericardium?

A

Restrains filling volume of heart

135
Q

What are the main causes of hypertension?

A

85% of people it is unknown
10% due to hyperaldosteronism
5% kidney disease, drugs, rare hormone excreting tumours

136
Q

If a patient presents with hypertension and hypokalaemia what is the most likely cause of the hypertension?

A

Hyperaldosteronism - potentially due to drugs

137
Q

What is the standard fall in blood pressure seen with the patient on one antihypertensive?

A

9mmHg

138
Q

How can a patient’s home BP be measured?

A

24 hour ambulatory blood pressure monitoring

139
Q

What is the threshold for requiring antihypertensive drugs in a patient with high blood pressure?

A

Depends on their risk

For low risk groups 160/100
For high risk groups 140/90

140
Q

What symptom is supposed to be dulled down by antihypertensive medication in a patient with high blood pressure?

A

Headache

141
Q

What BP are you aiming to achieve with medication and lifestyle changes in a hypertensive patient?

A

140/90 but tighter in diabetics

142
Q

How many drugs does it usually take in combination to achieve a ‘normal’ blood pressure in a hypertensive patient?

A

2-4

143
Q

What illnesses can be caused by HBP?

A

Dementia, stroke, peripheral vascular disease, aneurysm, renal failure, cardiovascular disease

144
Q

On average how much does hypertension shorten a patient’s life by?

A

7 years

145
Q

What is the percentage reduction in chance of having a stroke per 10mmHg dropped in blood pressure?

A

40%

146
Q

What are the main methods of lowering blood pressure without drug treatment?

A
  1. Reduce salt intake
  2. Lose weight
  3. Reduce alcohol consumption
147
Q

What are the main types of antihypertensive drugs?

A

A. ACE-I/ARB
B. Beta blocker
C. Calcium channel blocker
D. Diuretics

148
Q

What factors (unrelated to lifestyle) may contribute to high blood pressure?

A

Drugs (prescribed or not)

  • NSAIDs
  • COPC
  • SNRI’s (antidepressants)
  • Corticosteroids
  • Cold cures

Or/ recreational

  • Cocaine
  • Amphetamines
149
Q

In what circumstances should blood pressure lowering medication be withheld in a hypertensive patient?

A

Surgery

150
Q

How often should you monitor the blood pressure of a previously hypertensive patient on antihypertensive medication?

A

Every 6-12 months

151
Q

What are the 3 causes of aortic valve stenosis?

A
  1. Degeneration and calcification of normal valve
  2. Calcification of a congenital bicuspid valve
  3. Rheumatic heart disease
152
Q

How does aortic stenosis lead to angina, arrythmia and left ventricular failure?

A

Obstruction of left ventricular emptying, meaning increased afterload and so left ventricular hypertrophy.

This increases oxygen demand of heart until supply no longer meets demand and heart becomes ischaemic.

153
Q

How can aortic stenosis present?

A
  1. Angina
  2. Syncope
  3. Dyspnoea (and other symptoms of congestive HF) - most common symptom
154
Q

How severe must aortic stenosis be before symptoms present?

A

Orifice is normally 1/4 of normal size

155
Q

Explain why syncope is occasionally seen on exertion in patients with aortic stenosis

A

On exertion substances such as lactic acid and CO2 build up in muscles, stimulating parasympathetic nervous system to dilate vessels to allow more oxygen there, however this decreases blood pressure

CO can then not keep up with this vasodilation and individual loses consciousness

156
Q

What investigation is often diagnostic in aortic stenosis?

A

Echo
-Doppler examination of valve allowes assessment of pressure gradient across valve during systole as well as LV size and function

157
Q

What is classified as severe aortic stenosis?

A

Valve area <1cm squared

158
Q

What is the management for people with aortic stenosis?

A
  1. IE prophylaxis in medical and dental procedures
  2. Vasodilators relatively contraindicated if severe
  3. Surgical replacement
  4. TAVI (transcutaneous aortic valve implantation)
159
Q

What are the indications for aortic valve replacement in individuals with aortic stenosis?

A
  1. Symptomatic patients with severe
  2. Patients with severe AS undergoing CABG or surgery on aorta or other valves
  3. Patients with severe AS and depressed LVEF

OR/ in absence of symptoms: if valve area <= 0.6cm squared or if valve gradient exceeds 50mmHg on echo

160
Q

What is mitral regurgitation?

A

Backflow of blood from LV to LA during systole

161
Q

What are the most common causes of mitral regurgitation?

A
  1. In developed world - prolapsing mitral valve (myxomatous degeneration)
  2. In developing world - rheumatic heart disease
  3. Infective endocarditis
162
Q

How does mitral regurgitation often present?

A

Pulmonary oedema, due to pulmonary hypertension from increased pressure in left atrium.

Pulmonary hypertension can cause LV hypertrophy and LA enlargement in attempt to compensate, however often pulmonary hypertension will lead to right heart failure –> heart failure

163
Q

What are the physical signs on examination of an individual with mitral regurgitation?

A
  1. Soft S1, with pansystolic murmur (fills all of systole) at the apex and radiating into axilla
  2. Apex beat displaced laterally
  3. S3 often present
  4. Exercise intolerance (dyspnoea on exertion)
  5. HF
164
Q

Where do you auscultate all valves?

A

Aortic - Right 2nd intercostal space (sternum)
Pulmonary - Left 2nd intercostal space (sternum)
Tricuspid - Left 4th intercostal space (sternum)
Mitral - Left 5th intercostal space mid clavicular line

165
Q

What is rheumatic fever?

A

Inflammatory disease that occurs in children and young adults as a result of infection with group A B haemolytic streptococci. This causes an autoimmune reaction, and can impact heart valves.

166
Q

How does rheumatic heart disease present both clinically and on examination?

A
  1. 2-3 weeks after sore throat, acute onset
  2. Fever
  3. Joint pain
  4. Loss of appetite

On examination

  1. Changing heart murmurs/chest pain
  2. Polyarthritis
  3. Skin - erythema marginatum (transient pink rings) as well as small nodules over joints
  4. Sydenham’s chorea - Fidgety and sposmodic unintentional movement- involvement of CNS
167
Q

What criteria is used in the diagnosis of rheumatic fever?

A

Duckett Jones criteria

168
Q

What treatment is given in rheumatic fever?

A
  1. Bed rest
  2. High dose aspirin
  3. Penicillin to eradicate infection and long term to any with persistent damage
169
Q

What do splinting haemorrhages suggest?

A

Endocarditis

170
Q

What compensatory mechanisms does the body use in HF to maintain CO and peripheral perfusion?

A
  1. Increased sympathetic tone - improves ventricular function by increasing heart rate and contraction. It also contricts venous capacitance vessels meaning increased venous return to heart (preload) which further augments ventricular function (Starling)
  2. Fall in CO and increased sympathetic tone = diminished renal perfusion and activation on renin-angiotensin system and therefore increased fluid retention, which further increases venous pressure and maintains stroke volume.
171
Q

Why is oedema often seen in cardiac failure?

A

A fall in CO and increased sympathetic tone (which both occur in HF) leads to decreased renal perfusion and therefore activation of renin angiotensin system. This promotes sodium and water retention which in turn increases venous pressure and fluid retention.

172
Q

What are the two main differential diagnoses of DVT?

A

Cellulitis or HF

173
Q

What is the clinical presentation of DVT?

A

Pain, swelling, tenderness, warmth, discolouration

174
Q

What is the initial investigation carried out in suspected DVT? What is its significance?

A

D-dimer

Used for exclusion only - if normal: excludes DVT as can be raised in operation, pregnancy, inflammation.

175
Q

What is D-dimer test looking for in DVT?

A

Breakdown products of fibrin

176
Q

What things other than a clot can cause a D-dimer test to be raised?

A

Pregnancy, inflammation, operation

177
Q

If D-dimer came back raised in suspected DVT what would be the next investigation done?

A

Ultrasound compression test

178
Q

Ultrasound in DVT is the second investigation done after D dimer. In what case is the ultrasound useless?

A

If DVT is sitting in the calf. If they return a week later is likely to have moved proximally.

179
Q

What are the main risk factors for DVT?

A
  1. Surgery/immobility/leg fracture/POP
  2. OC pill, HRT, pregnancy (hypercoaguable in last trimester)
  3. Long haul flights/travel
  4. Inherited thrombophilia
180
Q

What is the treatment for a patient with confirmed DVT?

A
  1. LMW Heparin (s/c for min 5 days)
  2. Oral warfarin (DOAC) for 6 months if unclear cause, and 3 months if clear cause
  3. Compression stocking
  4. Treat underlying cause (if there is one)
181
Q

What is the difference in the length of time that oral warfarin is prescribed after a DVT when the cause is known compared to when the cause is unknown?

A

Cause known = 3 months

Cause unknown = 6 months

182
Q

In what groups of people in hospital should thromboprophylaxis be considered?

A

Hip and knee, pelvis, malignancy, prolonged immobility

183
Q

What are the signs and symptoms of PE?

and massive PE?

A

Pleuritic chest pain, breathlessness, signs of DVT sometimes, (risk factors), tachycardia, pleural rub, tachypneoa

Massive PE: hypotension, cyanosis, severe dyspnoea, right heart failure

184
Q

What are the initial investigations done in suspected PE?

And the gold standard further investigation (used to diagnose)

A
  1. CXR - abnormal in pneumonia, pneumothorax
  2. ECG - sinus tachy
  3. Blood gas - Type 1 resp failure (decreased Co2 and o2)

Gold standard = CTPA (pulmonary angiogram)

185
Q

What are the differential diagnosis of PE?

A

Lung cancer, pneumothorax, reflux, chest infection, musculoskeletal

186
Q

What is the treatment for PE?

A

Same as DVT:

  1. LMW Heparin (s/c for min 5 days)
  2. Oral warfarin (DOAC) for 6 months if unclear cause, and 3 months if clear cause
  3. Compression stocking
  4. Treat underlying cause (if there is one)
187
Q

Define population atrributable factor (PAF)

A

The proportion of the incidence of a disease in an exposed and non-exposed ppn that is due to an exposure, i.e. the disease incidence in the population that could be eliminated if the exposure were eliminated.

188
Q

What are the two biggest risk factors for CHD?

A

Cholesterol ratio ApoB/ApoA1

Smoking

189
Q

There are 2 main philosophical standpoints in explaining the pattern of CHD and who is affected by it. What are they called and outline their principles.

A
  1. Absolutist explanations e.g. Townsend score
    - It is about poverty and absolute measures of socioeconomic deprivation
  2. Relativist explanations e.g. Richard Wilkinson- Spirit Level
    - It is about relative differences, the larger the relative differences in society the poorer the outcomes and worse off for all e.g. infant mortality rates are higher in countries with high income inequality
190
Q

What is the effect of type A/B personality on the risk of CHD? Back this up with studies.

A

Type A:B 2:1 risk of CHD, found in both the Western collaborative group study and the Framington heart study

191
Q

What aspect of a Type A personality has been suggested to be the key risk factor in CHD?

A

Hostility

192
Q

What psychosocial job characteristics are associated with MI? What study backs this up?

A

High demand and low control

Whitehall studies - men in lowest grades had higher CHD risk

193
Q

What psychosocial factors could influence risk of CHD?

A
  1. Personality type (A/B)
  2. Work characteristics (over 11 hour days/ high demand and low control)
  3. Depression/anxiety
  4. Low social support
194
Q

Give 3 causes of left axis deviation

A

Often issue with LAD

  • LBBB
  • Left anterior fascicular block
  • Left ventricular hypertrophy
195
Q

Give 3 causes of right axis deviation

A
  • Left posterior fascicular block

- Right heart hypertrophy/strain

196
Q

T wave flattening or inversion is seen in?

A

Ischamia or hours after onset of STEMI

197
Q

If STEMI was inferior, what leads would it be seen in ?

A

II, III aVF

198
Q

If STEMI was septal what leads would it be seen in?

A

V1, V2

199
Q

Anterior infarct would be seen in leads?

A

V2-V6

200
Q

Lateral infarct would be seen in leads?

A

I, II, aVL

201
Q

What investigations would be done in suspected STEMI?

A

CXR, FBC, U&E, blood glucose and lipids, Cardiac markers (Troponin T and I and CK MB)

202
Q

What are the ECG changes in hyper and hypokalemia?

A

Hyper- Tall T waves, flattening of P waves, broadening of QRS
Hypo- Flattening of T wave and QT prolongation

203
Q

What are the ECG changes in hyper and hypocalcaemia?

A

Hyper - QT shortening

Hypo - QT prolongation

204
Q

What is the most common congenital heart defect?

A

Ventricular septal defect

Then ASD, PDA

205
Q

Is VSD a cyanotic or acyanotic CHD? and why

A

Acyanotic - High pressure LV and low pressure RV so blood flow from left to right –> increased blood flow through lungs

206
Q

VSD can lead to what?

A

Eisenmengers

207
Q

If VSD is small, what sign is still often present?

A

Loud systolic murmur and thrill

208
Q

Give 3 signs of a large VSD in an infant

A

Breathless, failure to thrive, poor feeding, large heart on xray, increased RR, tachycardia

209
Q

What is Eisenmengers?

A

Seen in VSD if large and left untreated. There is high pressure pulmonary blood flow, which leads to damage in pulmonary vasculature leading to increased resistance in the lungs
RV pressure then increases and shunt reverses
Child becomes cyanotic

210
Q

Give two examples of cyanotic CHDs?

A

Tetralogy of Fallot, Eisenmengers

211
Q

Give two examples of acyanotic CHD’s?

A

Ventricular septal defect, atrial septal defect

212
Q

ASD often presents in what age?

A

Adulthood

213
Q

VSD often presents in what age group?

A

Infants

214
Q

How do you treat a small ASD?

A

You don’t - leave (no symptoms)

215
Q

Signs of ASD?

A
  1. RH dilatation (big on xray)
  2. SOBOE
  3. Increased susceptibility of chest inf.
  4. Pulmonary flow murmur
  5. Fixed split second heart sound
  6. Big pulmonary arteries on CXR
216
Q

AVSD are often seen in patients with what disease?

A

Downs

217
Q

What is the malformation seen in AVSD?

A

One big malformed AV valve (rather than 2)

218
Q

How does an infant with AVSD present?

A

Breathless, failure to thrive, poor feeding and weight gain

219
Q

What are the 4 features typical of ToF?

A
  1. Overriding aorta
  2. Pulmonary stenosis
  3. Hypertrophy of R ventricle
  4. VSD
220
Q

What is the gene deletion that leads to ToF?

A

22q11

221
Q

ToF is normally resolved by what age?

A

2y

222
Q

Severity of illness in ToF greatly depends on what?

A

Severity of pulmonary stenosis - stenosis of RV outflow leads to RV being at higher pressure than the left –> cyanotic

223
Q

What is seen on CXR of patient with ToF?

A

Boot shaped heart

224
Q

What investigation is used to determine severity of stenosis in ToF?

A

Echo

225
Q

Give 3 clinical signs seen in ToF?

A
  1. Toddlers squat - increases PVD so degree of shunt reduced
  2. Difficulty feeding, failure to thrive and clubbing
  3. Adult patient - cyanosis
226
Q

What signs would indicate that patient required re-do surgery for TofF?

A
  1. Exertional dyspnoea
  2. Palpitations
  3. RV failure
  4. Syncope

Note/ can lead to sudden death

227
Q

In what direction is the shunt in PDA?

A

L–> R

228
Q

PDA is very common in what group of people?

A

Preterm babies

229
Q

What kind of murmur is heard in PDA?

A

Continuous ‘machinery’ murmur

230
Q

How does a baby with PDA appear?

A

Breathless, poor feeding, failure to thrive

231
Q

How is PDA treated?

A

Surgical or percutaneous closure

232
Q

What is coarctation of the aorta?

A

Narrowing of aorta at site of entry of ductus arteriosus

233
Q

What is the major complication in a severe coarctation of aorta?

A

Extreme HF –> death

234
Q

What are the clinical signs seen in coarctation of aorta?

A

Right arm hypertension
Bruits (buzzes)
Murmur

235
Q

Why are bicuspid AV valves an issue?

A
  1. Degenerate faster than normal valves
  2. Can be severely stenotic
  3. Associated with coarctation and dilation of ascending aorta
236
Q

What is pulmonary stenosis?

A

Narrowing of outflow of RV

237
Q

How does severe pulmonary stenosis present?

A
  1. RV failure as neonate
  2. RV hypertrophy
  3. Poor pulmonary blood flow
  4. Tricuspid regurg
238
Q

What is the Rx in pulmonary stenosis?

A
  1. Balloon valvuloplasty
  2. Open valvotomy
  3. Shunt
239
Q

Digoxin is indicated in which conditions?

A

HF + AF

OR HF (severe)

240
Q

How does digoxin work (mechanism)?

A

Inhibits Na/K pump

241
Q

What effects does digoxin have on body?

A
  1. Bradycardia
  2. Slows AV conduction
  3. Increases no. of ectopics
  4. Increases inotropic response
242
Q

Give 2 side effects of digoxin

A
  1. Nausea and vomiting
  2. Diarrhoea or constipation

V narrow therapeutic range

243
Q

What two drugs often cause QT prolongation and polymorphic ventricular tachycardia?

A

Amiodarone, sotalol

244
Q

Give 5 side effects of amiodarone

A
  1. Multiple drug interactions
  2. Interstitial pneumonitis
  3. Slate grey skin and sensitivity to sun
  4. Corneal microdeposits and optic neuropathy
  5. Hyper/hypothyroid
  6. Abnormal LFT

And very large volume of distrubution

245
Q

What is the difference between intermittent claudication and critical leg ischaemia?

A

Intermittent claudication - Pain on exertion, it is a moderate ischaemia often described as muscle cramp in the calf area. There is anaerobic metabolism when O2 demand exceeds supply. Lactic acid is formed and there is pain distal to atheroma.

Critical ischaemia - Pain at rest, typically lower down leg than calf. Often described as nocturnal and patient at risk of gangrene. There is dependency rubor. Blood supply is barely adequate to allow basal metabolism.

246
Q

What are the 6 P’s of acute ischaemia?

A

Pain, pale, pulseless, paraesthesia, paralysis, perishing cold

247
Q

What are the 4 stages of chronic limb ischaemia?

A
  1. Asymptomatic
  2. Intermittent claudication
  3. Rest pain/nocturnal pain
  4. Gangrene
248
Q

Briefly outline management of peripheral vascular disease (3 steps)

A
  1. Risk factor modification
  2. Revascularisation (vein bypass, percutaneous balloon angioplasty, stenting)
  3. Amputation
249
Q

Mechanism of streptokinase?

A

Plasminogen activator

250
Q

Investigations in suspected PVD?

A

History and examination
Ultrasound
Angiogram

251
Q

Most common causes of heart block?

A
  1. Coronary artery disease
  2. Cardiomyopathy
  3. Fibrosis of conducting tissue
252
Q

Difference in content of arterial and venous blood? - to do with drugs working there

A

Arterial - platelet rich (use antiplatelets)

Venous - fibrin rich - (use anticoag.)

253
Q

Mechanism of heparin?

A

Binds to antithrombin and increases activity

254
Q

How are mechanisms of aspirin and clopidogrel different?

A

Aspirin - Cox inhibitor, meaning that thromboxane production is inhibited, and hence there is platelet aggregation

Clopidogrel - inhibits ADP induced platelet aggregation

255
Q

How do NOAC’s work?

A

Work similarly to warfarin - Inhibit factors II and X

Clinical sciences (10 decks)

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